This work was supported by the University Hospitals Alzheimer Center and the USPHS grants AG08012 and AG10030 (RNK), and AG07552 and AG09287 (GP).
The Amyloid Precursor Protein in Ischemic Brain Injury and Chronic Hypoperfusiona
Article first published online: 17 DEC 2006
Annals of the New York Academy of Sciences
Volume 695, Alzheimer's Disease: Amyloid Precursor Proteins, Signal Transduction, and Neuronal Transplantation pages 190–193, September 1993
How to Cite
KALARIA, R. N., BHATTI, S. U., LUST, W. D. and PERRY, G. (1993), The Amyloid Precursor Protein in Ischemic Brain Injury and Chronic Hypoperfusion. Annals of the New York Academy of Sciences, 695: 190–193. doi: 10.1111/j.1749-6632.1993.tb23050.x
- Issue published online: 17 DEC 2006
- Article first published online: 17 DEC 2006
We studied changes in the spatial and temporal distribution of the β amyloid precursor protein (APP) of Alzheimer's disease (AD) in experimental ischemic brain injury. Rats with repeated reversible occlusions of one middle cerebral artery showed striking APP reactivity in astrocytic processes in perifocal regions and adjacent white matter. APP reactive dystrophic axons and neurons were also evident in the cortex and hippocampus ipsilateral to the MCA occlusion. Such changes were similarly apparent in animals subjected to partial forebrain ischemia induced by bilateral occlusion of the carotid arteries. Our studies suggest that focal ischemic insults or chronic hypoperfusion leads to increased accumulation or induction of APP in surviving cellular elements that may relate to the processes involved in β amyloid deposition in AD.